Gastric mucosa-associated lymphoma (GML) is a mature B cell tumor that accounts for 2-8% of all gastric cancers. Helicobacter pylori (H. pylori) infection is the main cause of GML, but the pathogenesis is not well understood. The genetic polymorphism of H. pylori is associated with the clinical outcome of infection. The clinical manifestation of GML are not specific, so GML commonly escapes diagnosis or is misdiagnosed, leading to excessive treatment. At present, there are no molecular markers for early GML diagnosis. Glycopeptidomics analyses of host cell lines (a BCG823 cell line, C823) and C823 cells infected by H. pylori isolated from patients with GML (GMALT823), gastritis (GAT823), gastric ulcer (GAU823) and gastric cancer (GAC823) were carried out to clarify the host reaction mechanism against GML and identify potential molecular criteria for the early diagnosis of GML. In total, 33 samples were analyzed and approximately 2000 proteins, 200 glycoproteins and 500 glycopeptides were detected in each sample. O-glycans were the dominant glycoforms in GMALT823 cells but not GAT823, GAU823 and GAC823 cells. Four specific glycoforms in GMALT823 cells and 2 specific glycoforms in C823 and GMALT823 cells were identified. Eight glycopeptides with specific glycosylation sites and the glycoforms of 7 glycoproteins were found in GMALT823 cells; of these glycopeptides, 6 specific glycopeptides have a high affinity for T cell epitopes and participate in cellular immunity, and 3 glycopeptides have conformational B cell epitopes and mediate liquid immunity. In this study, the relationship between the predominant glycoforms of host cells and the development of host disease was determined. Seven glycoproteins, 8 glycosylation sites and 9 glycoforms might be closely related to the formation of GML, which provides new insight into the pathogenic mechanisms of H. pylori infection and suggests molecular indicators for the early diagnosis of GML.